Increased Blood Glucose and Glucagon Stimulate the Secretion of Somatostatin

Somatostatin is first synthesized as a larger peptide precursor, preprosomatostatin. The hypothalamus also produces this protein, but the regulation of somatostatin secretion from the hypothalamus is independent of that from the pancreatic delta cells. Upon insertion of preprosomato-statin into the rough ER, it is initially cleaved and converted to prosomatostatin. The prohormone is converted into active hormone during packaging and processing in the Golgi apparatus.

Factors that stimulate pancreatic somatostatin secretion include hyperglycemia, glucagon, and amino acids. Glucose and glucagon are generally considered the most important regulators of somatostatin secretion.

The exact role of somatostatin in regulating islet hormone secretion has not been fully established. Somato-statin clearly inhibits both glucagon and insulin secretion from the alpha and beta cells of the pancreas, respectively, when it is given exogenously. The anatomic and vascular relationships of delta cells to alpha and beta cells further suggest that somatostatin may play a role in regulating both glucagon and insulin secretion. Although many of the data are circumstantial, it is generally accepted that somato-statin plays a paracrine role in regulating insulin and glucagon secretion from the pancreas.

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